CCS52A1/2 orchestrate hypocotyl endoreplication and elongation via PKN1/PKN2 pathways in Arabidopsis thaliana
Keywords:
CCS52A2, Cell expansion, Cell wall, Hypocotyl elongation, Lignin biosynthesisAbstract
Etiolated hypocotyls undergo rapid elongation compared with light-grown seedlings, a process associated with a developmental transition from mitotic cell division to endoreplication, resulting in increased cellular ploidy. CELL CYCLE SWITCH 52A2 (CCS52A2) is a key regulator of endoreplication in Arabidopsis thaliana, functioning through activation of the anaphase-promoting complex/cyclosome (APC/C) to mediate cyclin degradation. In this study, we demonstrate that loss-of-function mutations in CCS52A2 significantly reduce hypocotyl elongation, particularly under dark-grown (etiolated) conditions. Notably, this phenotype is partially rescued in a ccs52a2 pkn1 double mutant, indicating that CCS52A2 promotes etiolated hypocotyl elongation at least in part through the PKN1 signaling pathway. Furthermore, our findings suggest that endoreplication influences cell wall composition and its downstream modifications, providing new insight into the link between ploidy level and cell wall dynamics during skotomorphogenic growth.
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